Heart failure is a common course for the progression of many forms of heart disease. Heart failure may be considered to be the condition in which an abnormality of cardiac function is responsible for the inability of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues, or can do so only at an abnormally elevated filling pressure. There are many specific disease processes that can lead to heart failure, many of which are not fully known. In certain instances, heart disease may result from viral infections. In such cases, the heart may enlarge to such an extent that the adverse consequences of heart enlargement continue after the viral infection has passed and the disease continues its progressively debilitating course. In other cases, the initial cause is due to chronic hypertension, myocardial infarction, mitral valve incompetency, or other dilated cardiomyopathies. With each of these conditions, the heart is forced to overexert itself in order to provide the cardiac output demanded by the body during its various demand states. The result is dilation of the left ventricle and remodeling of the heart tissues.
Remodeling involves physical changes to the size, shape and thickness of the heart wall along with a neurohormonal milieu of the entire cardiovascular system. A damaged left ventricle may have some localized thinning and stretching of a portion of the myocardium. The thinned portion of the myocardium often is functionally impaired, and other portions of the myocardium attempt to compensate. As a result, the other portions of the myocardium may expand so that the stroke volume of the ventricle is maintained notwithstanding the impaired zone of the myocardium. Such expansion may cause the left ventricle to assume a somewhat spherical shape.
Cardiac remodeling often subjects the heart wall to increased wall tension or stress, which further impairs the heart's functional performance. Often, the heart wall will dilate further in order to compensate for the impairment caused by such increased stress. If dilation exceeds a critical value, the result will be progressive heart dilation which can be explained by Laplace's law. As the volume subtended by the left heart chamber increases, the stresses in the walls of this cavity will increase. Consequently, the muscle fibrils are overloaded and their ideal range of elongation is exceeded. When this excessive elongation takes place, there is a residual volume in the heart. Then the muscle fibrils must operate against a primarily high wall strain, and are further extended. A vicious cycle arises, leading to increasing distension of the heart and consequent heart insufficiency.
Heart transplantation is one surgical procedure used for treatment of heart failure. Unfortunately, not enough hearts are available for transplant to meet the needs of heart failure patients. In the United States, in excess of 35,000 transplant candidates compete for only about 2,000 transplants per year. A transplant waiting list is about 8-12 months long on average and frequently a patient may have to wait about 1-2 years for a donor heart. While the availability of donor hearts has historically increased, the rate of increase is slowing dramatically. Even if the risks and expense of heart transplant could be tolerated, this treatment option is becoming increasingly unavailable. Further, many patients do not qualify for heart transplant for failure to meet any one of a number of qualifying criteria.
Consequently, substantial effort has been made to find alternative treatments for heart failure. One such surgical treatment is referred to as the Batista procedure; the surgical technique includes dissecting and removing portions of the heart in order to reduce heart volume. This is a radical and experimental procedure subject to substantial controversy. Furthermore, the procedure is highly invasive, risky and expensive and commonly includes other expensive procedures (such as a concurrent heart valve replacement). And if the procedure fails, emergency heart transplant is the only available option.
Another surgical treatment is dynamic cardiomyoplasty. In this procedure, the latissimus dorsi muscle (taken from the patient's shoulder) is wrapped around the heart and chronically paced synchronously with ventricular systole. Pacing of the muscle results in muscle contraction to assist the contraction of the heart during systole. Even though cardiomyoplasty has demonstrated symptomatic improvement, studies suggest the procedure only minimally improves cardiac performance. In addition, the procedure is highly invasive requiring harvesting a patient's muscle and an open chest approach (i.e., sternotomy) to access the heart. Furthermore, the procedure may be expensive and complicated. For example, it is difficult to adequately wrap the muscle around the heart with a satisfactory fit. Also, if adequate blood flow is not maintained to the wrapped muscle, the muscle may necrose. The muscle may stretch after wrapping reducing its constraining benefits and is generally not susceptible to post-operative adjustment. Finally, the muscle may fibrose and adhere to the heart causing undesirable constraint on the contraction of the heart during systole.
A variety of devices have also been developed to treat heart failure by improving cardiac output. For example, left ventricular assist pumps have been developed to help the heart to pump blood. These mechanical pumps reduce the load on the heart by performing all or part of the pumping function normally done by the heart. Currently, mechanical pumps are used to sustain the patient while a donor heart for transplantation becomes available for the patient. Researchers and cardiac surgeons have also experimented with prosthetic “girdles” disposed around the heart. One such design is a prosthetic “sock” or “jacket” that is wrapped around the heart. However, these designs require invasive open chest surgery, significant handling of the heart, and have not seen widespread success.
Heart failure may also be caused by electrical conduction delay or blockage within the heart. For example, approximately 30% to approximately 50% of patients with congestive heart failure have interventricular conduction defects often in the pattern of a left bundle branch block (LBBB). These conduction abnormalities lead to a discoordinated contraction of an already failing and inefficient heart. Even a delayed activation of the left ventricle when the right ventricle alone is paced, for example, leads to significant dyssynchrony in left ventricular contraction and relaxation. The result is further deterioration of left ventricular performance because of abnormal septal motion, altered diastolic filling parameters, and alteration of heart geometry that may lead to worsening mitral regurgitation.
In recent years many new pacing and defibrillator devices with special algorithms have been proposed to alleviate heart failure conditions and restore synchronous depolarization and contraction of a single heart chamber or a combination of right/left and upper/lower heart chambers.
In patients who receive right-sided dual chamber pacemakers (e.g., pacemakers that include right atrial and right ventricular leads) for bradycardia indications, adjusting the timing intervals (e.g., in conjunction with echocardiographic Doppler filling characteristics) occasionally improves functional class (also referred to as New York Heart Association (NYHA) functional class) by optimizing cardiac output and diastolic filling parameters. Generally, however, attempts to resynchronize ventricular activation with traditional right sided pacing have not been very successful.
Strategies to correct dyssynchrony have led to technological advances in pacemaker therapy. Unlike traditional right-sided pacing, cardiac resynchronization devices may also use a left ventricular lead usually placed distally in the coronary sinus so that both ventricles are depolarized simultaneously. The synchronized activation improves overall cardiac function.
It has been proposed that biventricular pacing pulses be applied simultaneously to the right and left ventricles. Generally, the exact timing of mechanical events allows for properly controlling right and left heart chamber pacing so as to optimize left ventricular output. Specifically, it is known that actual contraction of one ventricular chamber before the other has the effect of moving the septum so as to impair full contraction in the later activated chamber. Thus, while concurrent or simultaneous pacing of the left and right ventricle may achieve a significant improvement for patients with congestive heart failure, it may be better to provide for pacing of the two ventricles in such a manner that the actual mechanical contraction of the left ventricle, with the consequent closing of the left valve, occurs in a desired time relationship with respect to the mechanical contraction of the right ventricle and closing of the right value. For example, if conduction paths in the left ventricle are impaired, delivering a pacing stimulus to the left ventricle at precisely the same time as delivering a pacing stimulus to the right ventricle may nonetheless result in left ventricular contraction being slightly delayed with respect to the right ventricular contraction.
Biventricular pacing includes traditional placement of a pacing lead in the right ventricle and placement of an additional pacing lead on the epicardial surface of the left ventricle. This is performed in an effort to resynchronize the contraction of the left ventricle. Placing a lead in the cavity of the left ventricle may result in complications due to thromboembolization, as thrombi frequently form on the surface of the left ventricle lead. Thus, to reduce or avoid thromboembolization, the left ventricle lead may be placed epicardially on the surface of the left ventricle.
In early use of biventricular pacing, the left ventricle leads were placed via a thoracotomy or through a thoracoscopy. Understandably these procedures may add significantly to the morbidity and mortality of already sick patients. Subsequently, a technique was developed that includes positioning a pacing wire on the surface of the left ventricle transvenously. The venous return from the myocardium includes multiple veins located on the surface of the heart that join to form the coronary sinus (CS). The CS then drains into the right atrium. It is possible to cannulate the CS from the right atrium and retrogradely place a pacing lead that is then positioned into one of its branches on the surface of the left ventricle.
Generally, however, conventional pacing systems require multiple lead placements. Further, due to an inability to directly stimulate the left heart, conventional pacing systems include high energy requirements that may cause early battery drainage with subsequent early battery replacement.